A model of Alexander disease found glutathione-independent protective effects of GFAP-Nrf2 expression66, and a proteomic study of Nrf2-overexpressing astrocytes found important roles of detoxifying and anti-inflammatory enzymes catalase, peroxiredoxin-6 and prostaglandin reductase 167 which could alternatively be implicated following hypoperfusion as opposed to increased glutathione synthesis. This evidence concerns the gene GFAP and Alexander disease.